Mitochondrial redox system: A key target of antioxidant therapy to prevent acquired sensorineural hearing loss

Jeong-In Baek1, Ye-Ri Kim2,3, Kyu-Yup Lee4

  • 1Department of Companion Animal Health, College of Rehabilitation and Health, Daegu Haany University, Gyeongsan, Republic of Korea.

Insights

Protecting hearing from noise and drugs involves understanding oxidative stress. This review explores targeting mitochondrial redox networks to prevent or treat acquired sensorineural hearing loss.

Area of Science:

  • Oto-pharmacology
  • Neuroscience
  • Cellular Biology

Background:

  • Acquired sensorineural hearing loss stems from noise, ototoxic drugs, and aging.
  • Oxidative stress, particularly mitochondrial reactive oxygen species (ROS) imbalance, is a key factor in hearing loss.
  • Current research focuses on protecting cochlear hair cells and auditory nerves.

Purpose of the Study:

  • To review the potential of targeting mitochondrial redox networks for hearing loss prevention and treatment.
  • To explore therapeutic strategies against noise- and drug-induced ototoxicity.
  • To highlight the role of antioxidants in maintaining hearing function.

Main Methods:

  • Literature review of pathological mechanisms in acquired hearing loss.
  • Analysis of the role of mitochondrial redox homeostasis in auditory cells.
  • Investigation of antioxidant strategies against ototoxic stimuli.

Main Results:

  • Mitochondrial ROS imbalance is implicated in acquired sensorineural hearing loss.
  • Antioxidants show promise in supporting auditory cell function.
  • Targeting specific elements of the mitochondrial redox network is a viable therapeutic avenue.

Conclusions:

  • Developing drugs targeting the mitochondrial redox network offers a promising strategy for preventing and treating noise- and ototoxic drug-induced hearing loss.
  • Further research into redox homeostasis in hair cells is crucial.
  • Antioxidant therapies hold potential for preserving hearing function.

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